Declaration of National Alzheimer's Disease Month Awareness of Alzheimer's disease increases, leading Congress to designate November 1983 as the first National Alzheimer's Disease Month. 1984 Beta-amyloid identified Researchers George Glenner and Cai'ne Wong report identification of "a novel cerebrovascular amyloid protein," known as beta-amyloid — the chief component of Alzheimer's brain plaques and a prime suspect in triggering nerve cell damage. 1984 Nationwide infrastructure for Alzheimer's research established The NIA begins funding its network of Alzheimer's Disease Centers at flagship medical institutions, establishing a nationwide infrastructure for research, diagnosis and treatment. 1986 1986 Tau protein identified Researchers discover that tau protein is a key component of tangles—the second pathological hallmark of Alzheimer's disease and another prime suspect in nerve cell degeneration. 1987 First Alzheimer's drug trial The Alzheimer's Association assists the NIA and Warner-Lambert Pharmaceutical Company (now Pfizer) in launching and recruiting participants for clinical trials of tacrine, the first drug specifically targeting symptoms of Alzheimer's disease. 1987 First deterministic Alzheimer's gene identified Researchers identify the first gene associated with rare, inherited forms of Alzheimer's disease .

This gene on chromosome 21 codes amyloid precursor protein (APP), the parent molecule from which beta-amyloid is formed. Chromosome 21 is also the chromosome of which those with Down syndrome have three copies rather than two. Many individuals with Down syndrome develop Alzheimer's disease, often as young as their 30s and 40s. Federal clinical study consortium launched The National Institute on Aging (NIA) established the Alzheimer's Disease Cooperative Study (ADCS), a nationwide medical network to facilitate clinical research and conduct federally funded clinical trials. 1993 First Alzheimer's risk factor gene identified Researchers identify APOE-e4 , a form of the apolipoprotein-E (APOE) gene on chromosome 19, as the first gene that raises risk for Alzheimer's but does not determine that a person who has it will develop the disease. 1993 First Alzheimer's drug approved by FDA The Food and Drug Administration (FDA) approves tacrine (Cognex) as the first drug specifically targeting Alzheimer's memory and thinking symptoms. Four additional drugs are approved over the next 10 years. 1994: President Reagan's diagnosis announced Former U.S.

President Ronald Reagan shares with the American people that he has been diagnosed with Alzheimer's disease. First World Alzheimer's Day The first World Alzheimer's Day (WAD) launches on September 21 by Alzheimer's Disease International, the umbrella organization of Alzheimer's associations. 1995 First transgenic mouse model announced Researchers announce the first transgenic mouse model that developed Alzheimer-like brain pathology. The mouse was developed by inserting one of the human APP genes linked to a rare, inherited form of Alzheimer's disease. The Alzheimer's Association first awarded a grant to develop a mouse model of a rare neurodegenerative disorder called Gerstmann-Sträussler-Scheinker syndrome in 1989, laying the technical foundation for Alzheimer's mouse models. 1999 "Alzheimer's vaccine" successful in mice The first in a series of reports is published showing that injecting transgenic "Alzheimer" mice with beta-amyloid prevents the animals from developing plaques and other Alzheimer-like brain changes.

Genetics Study begins The Alzheimer's Association partners with the National Institute on Aging to recruit participants for the National Alzheimer's Disease Genetics Study, a federal initiative to collect and bank blood samples from families with several members who developed Alzheimer's disease late in life in order to identify additional Alzheimer's risk genes. 2004 First report on Pittsburgh Compound B (PIB) Researchers at the Alzheimer's Association International Conference on Alzheimer's Disease (AAICAD) share their first report on an imaging agent called Pittsburgh Compound B (PIB), a major potential breakthrough in disease monitoring and early detection. PIB enters the brain through the bloodstream and attaches itself to beta-amyloid deposits, where it can be detected by positron emission tomography (PET). The Alzheimer's Association provided significant support to initiatives to develop PIB and conduct preclinical testing it in animal studies. 2004: Alzheimer's Disease Neuroimaging Initiative (ADNI) The Alzheimer's Association joins public and private donors as a major sponsor of the Alzheimer's Disease Neuroimaging Initiative (ADNI) , a nationwide study to establish standards for obtaining and interpreting brain images. Healthy Brain Initiative launched The Alzheimer’s Association and the U.S.

Centers for Disease Control and Prevention launch the Healthy Brain Initiative with the publication of A National Public Health Road Map to Maintaining Cognitive Health. The Road Map advances 44 science-based actions emphasizing primary prevention of cognitive impairment. The goal of this initiative is to maintain or improve the cognitive performance of all adults. 2008 International Society to Advance Alzheimer Research and Treatment formed To further the work of the global Alzheimer's research community, the Alzheimer's Association creates the International Society to Advance Alzheimer's Research and Treatment (ISTAART) , the first and only professional society dedicated to Alzheimer's and Dementia. 2009 International Conference on Alzheimer's Disease becomes an annual event raise awareness and concern Dozens of Alzheimer's researchers unite with the Alzheimer's Association for an "Alzheimer's Breakthrough Ride®," a 66-day bike relay across America to raise public and congressional awareness of the urgent need for more federal funding to support the search for effective Alzheimer's treatments. 2010 database established The Alzheimer's Association and its partners in the Coalition Against Major Diseases (CAMD) released a first-of-its kind database of 4,000 patients who participated in 11 pharmaceutical industry-sponsored clinical trials of Alzheimer's treatments.

The combined data, accessible to any qualified researcher, will offer unprecedented power to understand the course of Alzheimer's. 2010 TrialMatch® launched The Association launches TrialMatch ®, a free, user-friendly tool to help prospective participants identify clinical studies that might be a good fit. Stakeholders have unanimously identified building awareness of studies and increasing enrollment as key strategies to accelerate treatment development. 2010 sixth-leading cause of US deaths The Centers for Disease Control and Prevention (CDC) National Center for Health Statistics releases final 2007 data showing that Alzheimer's disease is now our sixth-leading cause of death. 2010 An influential model of biomarker changes during Alzheimer’s disease progression is first published A group of researchers publish a working model relating changes in Alzheimer’s biomarkers to disease stage and symptom severity. The model has become a focal point of research into Alzheimer’s biomarkers, and is revised periodically to account for new research. 2011 National Alzheimer's Project Act (NAPA) into law Groundbreaking legislation establishes our first-ever framework for a national strategic plan to address the Alzheimer's crisis and to coordinate our response on multiple fronts, including research, care and support.

New criteria and guidelines for Alzheimer's disease diagnosis Three workgroups convened by the Alzheimer's Association and the National Institute on Aging issue updated criteria and guidelines for diagnosing Alzheimer's disease and propose a research agenda to define a new preclinical stage. 2011 Annual assessment for cognitive impairment for all Medicare Beneficiaries implemented as part of Annual Wellness visits The Centers for Medicare and Medicaid Services implement Annual Wellness Visits for all Medicare Beneficiaries under the Patient Protection and Affordable Care Act. A mandatory part of the Annual Wellness Visit is an assessment for detection of cognitive impairment. 2012 First major clinical trial for prevention of Alzheimer’s disease is initiated A multinational research consortium, the Dominantly Inherited Alzheimer Network, launches the first major clinical trial testing drug therapy to prevent the onset of Alzheimer’s disease symptoms in people who inherited an autosomal dominant mutation putting them at high risk for the disease. 2013 International Genomics of Alzheimer’s Project (IGAP) researchers identify new genetic risk factors for Alzheimer’s disease Hundreds of researchers from around the world collaborate to perform a meta-analysis of genome-wide association studies intended to identify genetic variations linked with an increased risk for Alzheimer’s disease.

The collaboration revealed 20 genetic variations associated with increased risk, 11 of which had not been linked with Alzheimer’s before. Some of the newly identified genetic variations are thought to be specific to the immune system, adding to mounting evidence of a role for the immune system in Alzheimer’s disease. 2014 Rates of death caused by Alzheimer’s disease found to be much higher than reported on death certificates Researchers at Rush University find that the annual number of deaths attributable to Alzheimer’s disease in the U.S. among people at least 75 years old is about 500,000, much higher than the number reported on death certificates (<84,000). Alzheimer's Disease News | Wiki - UPI.com Alzheimer's Disease News Next Wiki Alzheimer's disease (AD), also called Alzheimer disease, Senile Dementia of the Alzheimer Type (SDAT) or simply Alzheimer's, is the most common form of dementia. This incurable, degenerative, and terminal disease was first described by German psychiatrist and neuropathologist Alois Alzheimer in 1906 and was named after him.

Generally it is diagnosed in people over 65 years of age, although the less-prevalent early-onset Alzheimer's can occur much earlier. An estimated 26.6 million people worldwide had Alzheimer's in 2006; this number may quadruple by 2050. Although each sufferer experiences Alzheimer's in a unique way, there are many common symptoms. The earliest observable symptoms are often mistakenly thought to be 'age-related' concerns, or manifestations of stress. In the early stages, the most commonly recognised symptom is memory loss, such as difficulty in remembering recently learned facts. When a doctor or physician has been notified, and AD is suspected, the diagnosis is usually confirmed with behavioural assessments and cognitive tests, often followed by a brain scan if available. As the disease advances, symptoms include confusion, irritability and aggression, mood swings, language breakdown, long-term memory loss, and the general withdrawal of the sufferer as their senses decline. Gradually, bodily functions are lost, ultimately leading to death. Individual prognosis is difficult to assess, as the duration of the disease varies. AD develops for an indeterminate period of time before becoming fully apparent, and it can progress undiagnosed for years.

The mean life expectancy following diagnosis is approximately seven years. Fewer than three percent of individuals live more than fourteen years after diagnosis. The cause and progression of Alzheimer's disease are not well understood. Research indicates that the disease is associated with plaques and tangles in the brain. Currently used treatments offer a small symptomatic benefit; no treatments to delay or halt the progression of the disease are as yet available. As of 2008, more than 500 clinical trials were investigating possible treatments for AD, but it is unknown if any of them will prove successful. Many measures have been suggested for the prevention of Alzheimer's disease, but their value is unproven in slowing the course and reducing the severity of the disease. Mental stimulation, exercise, and a balanced diet are often recommended, as both a possible prevention and a sensible way of managing the disease. Important Things to know about Alzheimer's and Dementia Care - Dorson Home Care / News & Events /by Dorsonhome Alzheimer’s was first described & named after a German Psychiatrist / Neuropathologist Alois Alzheimer in 1906. Alzheimer’s is a form of Dementia (loss of mental skills), which significantly affects behavior, thinking and memory.

It can affect any age group. It tends to be more prominent in ages 65 and older. Some causes include: genetics, nutritional deficiencies, poor eating habits, stress, brain and head injuries,kidney & liver diseases & strokes as well as sensory loss in eyes and ears causing confusion. There are multiple symptoms which affect daily living, such as: cognitive & speech difficulties, difficulties remembering recent events, places and things, deterioration in thinking abilities, severe memory loss, mood swings and personality changes and withdrawal from work, social activities, family & friends Healthy tips for your loved ones with Alzheimer’s and Dementia: Be calm, flexible and guiding (not controlling) Engage in activities such as exercise, massage & yoga Help them develop healthy eating diets and habits Take advantage of mental stimulation via arts & crafts, card & word games, crossword puzzles, gardening, light dancing & music, reading and other recreational activities Allow regular visits from close friends & family Dress them in their favorite accessories and attire Alzheimer’s and Dementia Care can be very stressful for caregivers, including the spouse, child, close relative or friend. In addition, many caregivers are faced with taking care of their loved ones with Alzheimer’s and Dementia at home.

Choosing an accredited/compassionate/ reputable home care provider can help ease this burden and provide peace of mind. For details on an experienced NJ Home Care provider with a team of Certified Dementia Practitioners and specialized seminars on Alzheimer’s and Dementia, please check out these links: Title page for ETD etd-08162010-102550 Title page for ETD etd-08162010-102550 Type of Document etd-08162010-102550 Title A Study of the Elongation of Fibrils of the Alzheimer's Amyloid Beta Protein with a Coarse-Grained Force Field Degree simulations Date of Defense 2010-07-12 Availability unrestricted Abstract Alzheimer�s disease (AD) is a brain disorder named after the German psychiatrist Alois Alzheimer, who first described the disease in 1906. AD is a form of dementia, characterized by impairment of memory and other intellectual abilities, caused by the loss of neurons and synapses (the structures that permit communication between neurons) in certain regions of the brain.

Although the mechanism by which neurons are affected is not yet well understood, research points to a small protein, the beta-amyloid peptide (Abeta), as the first suspect. Ab chains are present in the brains of healthy individuals, but in AD patients, they associate and form clumps that deposit outside neurons, and are believed to trigger the disease. In this dissertation, I use computational methods to study the behavior of the structures formed by Ab chains, when they associate with each other, and how these structures grow. The goal of this work is to use computational methods to complement experimental results by filling the gaps about structural and association mechanism that cannot be accessed by experiments. Files Lead Exposure & Alzheimerï¿½s Disease: Is There A Link? Lead Exposure & Alzheimerï¿½s Disease: Is There A Link? A fact sheet for medical professionals by Dr. Iman Hegazi, MBBS, MD. Forensic Medicine & Toxicology, Global Lead Advice & Support Service (GLASS), run by The LEAD Group Inc Alzheimer's disease (AD), or simply Alzheimer's, is the most common form of dementia.

This incurable, degenerative, and terminal disease was first described by German psychiatrist and neuropathologist Alois Alzheimer in 1906 and was named after him. (1) Generally it is diagnosed in people over 65 years of age, although the less-prevalent early-onset Alzheimer's can occur much earlier. An estimated 26.6 million people worldwide had Alzheimer's in 2006; this number may quadruple by 2050. (2, 3) The term "Alzheimerï¿½s" is rapidly being used by the general public to refer to any elderly person suffering from dementia. Everyone who suffers from Alzheimer's disease has dementia. However, not everyone with dementia has Alzheimer's disease. Dementia may be caused by several other diseases. History: Alzheimerï¿½s disease, the chronic decline in intellectual capabilities, was recognized by the ancient Greek physician Hippocrates. At the time "senility" was thought to be simply a normal part of aging (4). Alois Alzheimer, better defined the disease in a speech given in November 1906. Dr.

Alzheimer examined the brain, after her death, of a woman who died at the age of 56, after having paranoid delusions, hallucinations, and a loss of memory, and noticed senile plaques and neurofibrillary tangles in the neurons (brain cells) (5). Alzheimer wrote, "On the whole, it is evident that we are dealing with a peculiar, little known disease process." Up until 1970 the diagnosis of Alzheimerï¿½s disease was restricted to patients less than 65 years old(4). Alzheimerï¿½s disease is no longer defined by age with between 50% and 75% of all dementia cases now being diagnosed as Alzheimerï¿½s disease, with the proportion increasing with age (6,7). Overview of Changes in the Brain: Alois Alzheimer was able to describe two of the major changes in brain structure caused by Alzheimerï¿½s disease. In addition to the neurofibrillary tangles and neuritic plagues, AD also results in granulovascular degeneration, brain shrinkage, and decreased amounts of neurotransmitters (brain chemicals involved in communication).

All of these changes impair the function of brain cells (neurons) and eventually lead to cellular death. Unlike many other cells, the brain is unable to regenerate new neurons. The gradual and progressive death of neurons is mirrored in specific behaviour changes. (4) Phases of Alzheimer's Mild dementia The chief characteristic of mild Alzheimerï¿½s disease is forgetfulness. Not only will the individual misplace items but will start to place them in unusual locations (e.g. keys in the freezer). The decline may be so gradual that it may take family members years to notice since some forgetfulness is a natural part of aging. Loss of a sense of time and direction greatly interferes with the ability to navigate and are important components of a "sense of direction." The characteristic of becoming lost, especially in unfamiliar territory is a common hallmark in mild AD. (4) Moderate dementia Once Alzheimerï¿½s disease deteriorates to the moderate stage; profound memory loss that interferes with daily activities characterizes the disorder. The AD patient in the moderate stage is dependent upon others. The sufferer becomes lost even in familiar surroundings and has lost the ability to learn any new material.

(4) Severe dementia Once the disease progresses to the severe stage the patient suffers from severe impairment of mind (cognitive functions) and body. The subject has reached the point they may no longer recognize their spouse and children. The AD patient no longer has any sense of time or current location. Verbal communication has decreased to the point of phrases, words, or merely syllables are constantly repeated. Eventually, even this simple communication degenerates to a complete inability to speak. The overall loss of coordination and body control means the patient may require help dressing, bathing, grooming, eating, and toileting. (4) Description: Combination of two diagrams of the brain in one for comparison. Left: A normal brain. Right: The brain of a person with Alzheimer's disease showing extreme shrinkage of the cerebral cortex and hippocampus and enlargement of the ventricles. (8) The copyright holder of this work grant anyone the right to use this work for any purpose , without any conditions, unless such conditions are required by law. Although Alzheimerï¿½s disease (AD) is a progressive neurodegenerative disorder whose clinical manifestations appear in old age, the initial events that trigger this disease may begin very early in life.

In consequence of the ï¿½Barker hypothesisï¿½, which links early life experiences and adult diseases, there is a new concept regarding certain adult diseases that emphasizes the role of environmental factors operating during the preconceptual, fetal, and infantile phases of life. (9) The sporadic nature of most AD cases strongly argues for an environmental link that may accelerate normal age-related processes in the brain. Due to the widespread occurrence of AD, such environmental agents (risk factors) would have to be widespread and persistent, and chronic human exposure to them very common. Although few environmental agents may fit this description, the heavy metal Pb is widespread and is known to produce permanent behavioral and cognitive perturbations. (10, 11) Lead (Pb) poses widespread public concern. Humans can be exposed to Pb through paint, glazed earthenware, lead piping, solder in food containers, moonshine whiskey, and automobile battery casings. Occupational exposure to Pb can come from smelters, battery manufacturing, welding, automobile radiator repair, and production of Pb-based paints. Although organic forms of Pb have been removed from gasoline, inorganic Pb still remains the number one environmental hazard facing humans today.

(12) Occupational lead exposure may have long-term effects and dramatically increase the risk of developing Alzheimer's disease in later years, according to research presented during the American Academy of Neurology's 52nd Annual Meeting in San Diego, CA, April 29 -- May 6, 2000. Researchers believe that people who have worked in jobs with high levels of lead exposure are up to 3.4 times more likely to develop Alzheimer's disease. Dr Koss of the American Academy of Neurology quotes: "Although lead has long been known to be toxic -- and is believed to have affected the brains of some of the rulers of the Roman Empire, thereby causing its downfall -- its long-term damages are difficult to measure, and thus, the extent of its negative effects have been largely overlooked." (13) The pathogenesis of Alzheimerï¿½s disease: Evidence for an environmental link: AD pathology is characterized by senile plaques and neurofibrillary tangles (NFTs), combined with massive neuronal loss.

The major constituents of senile plaques (or amyloid plaques) are 39ï¿½42 residue peptides (Aβ) snipped from a larger protein called the amyloid precursor protein (APP). Current studies indicate that APP is processed by a group of secretases. Cleavage of APP by β-secretase produces sAPPβ and C99 fragments. C99 is then cleaved by γ-secretase to release Aβ. However, prior processing of APP by α-secretase precludes the formation of the neurotoxic Aβ. Inhibiting α- secretase activity predisposes the processing of APP via the β-secretase pathway, which ultimately leads to neurotoxicity. On the other hand, suppression of β-secretase or γ-secretase activity prevents the formation of the neurotoxic Aβ molecule. (14,15) Aβ processing and aggregation are thought to be critical events in the etiology of neurodegenerative diseases such as AD. Mutations in APP have been shown to promote AD pathogenesis in familial AD by altering its proteolytic processing, which results in an increased production of Aβ.

(16) Recent studies in rodents have shown that exposure to lead (Pb) during brain development predetermined the expression and regulation of the amyloid precursor protein (APP) and its amyloidogenic β-amyloid (Aβ) product in old age. It is also reported that the expression of AD-related genes [APP, BACE1] as well as their transcriptional regulator (Sp1) were elevated in 23-year-old monkeys exposed to Pb as infants leading to an Alzheimer's disease (AD)-like pathology in the aged monkeys. (17, 18) Chronic lead (Pb) exposure also affected granule cell morphology in Pb-exposed rats. Dendrites frequently appeared dystrophic, similar to those present in Alzheimerï¿½s disease. Dendrites play an essential role in neuronal signaling and aberrations in dendritic morphology are likely to alter their functional characteristics. (19) These data suggest that AD pathogenesis is influenced by early life exposures and argue for both an environmental trigger and a developmental origin of AD. The findings implicate an environmental agent (Pb) in the pathogenesis of AD and demonstrate that development is an important period of vulnerability, which could increase future susceptibility to neurodegeneration and AD pathology.

Therapeutic proof of heavy metal implication: Clioquinol, a chelating agent used in heavy metal toxicity, is under investigation for the treatment of Alzheimer disease. A pilot phase 2 study with clioquinol showed that the effect of the treatment was significant in the more severely affected group and supports further investigation of this novel treatment. Clioquinol is a chelator that crosses the blood-brain barrier and may diminish the accumulation of amyloid beta in plaques. Clioquinol was shown to produce a significant reversal of amyloid-beta plaque deposition in vitro as well as in vivo in a clinical trial. (20, 21) Another pilot study has shown the efficacy of the chelating agent d-penicillamine in reducing oxidative stress in Alzheimer disease patients. (22) In conclusion, lead (Pb) is a xenobiotic metal with no known essential function in cellular growth, proliferation, or signalling and there is compelling evidence that exposures to Pb have adverse effects on the nervous system. (23) The sporadic nature of Alzheimer's disease (AD) and a number of studies suggest that AD pathogenesis is influenced by early life exposures and argue for both an environmental trigger and a developmental origin of AD.

Recent research presents novel findings that implicate lead (Pb) in the pathogenesis of AD and demonstrate that development is an important period of vulnerability, which could increase future susceptibility to neurodegeneration and AD pathology. References Berchtold NC, Cotman CW (1998). "Evolution in the conceptualization of dementia and Alzheimer's disease: Greco-Roman period to the 1960s". Neurobiol. Aging 19 (3): 173ï¿½89. doi : 10.1016/S0197-4580(98)00052-9 . PMID 9661992 . Police Found This Alzheimer's Patient Wandering Alone, What He Was Doing Is Simply Stunning Police Found This Alzheimer's Patient Wandering Alone, What He Was Doing Is Simply Stunning SHARE Alzheimer’s disease (AD) is the most common form of dementia. It was first described by (and later named after) German psychiatrist and neuropathologist Alois Alzheimer in 1906.

Most often, AD is diagnosed in people over 65 years of age, In 2010, there were 28.6 million people worldwide with AD. Sadly, the guy in the video is a sufferer. I’m not. And yet I’ve been known to forget my girlfriends birthday until Facebook reminded me. It’s common for guys to sometimes forget their spouse’s birthday or Mother’s Day, but when you’ve been diagnosed with Alzheimer’s, it’s particularly rough. When you can’t remember the name of your loved ones, it’s hard to be expected to remember special dates, but sometimes miraculous things happen. Melvyn is living with Alzheimer’s, but recently he gave his wife the surprise of her life. Go grab a tissue and take a look. I can’t even imagine the devastation that Alzheimers brings to a family, so it’s inspiring to see Melvyn’s courageous battle against the disease…. long may it continue.

Alzheimer’s Disease Treatment, Abu Dhabi | ACPN, Dubai, Sharjah / Health Education Center / Adult / Adult – A / Alzheimer’s Disease (AD) Alzheimer, also called Alzheimer disease, Senile Dementia of the Alzheimer Type (SDAT) or simply Alzheimer’s, is the most common form of dementia. This incurable, degenerative, and terminal disease was first described by German psychiatrist Alois Alzheimer in 1906 and was named after him. Generally it is diagnosed in people over 65 years of age, although the less-prevalent early-onset Alzheimer’s can occur much earlier. An estimated 26.6 million people worldwide had Alzheimer’s in 2006; this number may quadruple by 2050. Although each sufferer experiences Alzheimer’s in a unique way, there are many common symptoms. The earliest observable symptoms are often mistakenly thought to be ‘age-related’ concerns, or manifestations of stress. In the early stages, the most commonly recognised symptom is memory loss, such as difficulty in remembering recently learned facts. When a doctor or physician has been notified, and AD is suspected, the diagnosis is usually confirmed with behavioural assessments and cognitive tests, often followed by a brain scan if available.

As the disease advances, symptoms include confusion, irritability and aggression, mood swings, language breakdown, long-term memory loss, and the general withdrawal of the sufferer as their senses decline. Gradually, bodily functions are lost, ultimately leading to death. Individual prognosis is difficult to assess, as the duration of the disease varies. AD develops for an indeterminate period of time before becoming fully apparent, and it can progress undiagnosed for years. The mean life expectancy following diagnosis is approximately seven years. Fewer than three percent of individuals live more than fourteen years after diagnosis. The cause and progression of Alzheimer’s disease are not well understood. Research indicates that the disease is associated with plaques and tangles in the brain. Currently-used treatments offer a small symptomatic benefit; no treatments to delay or halt the progression of the disease are as yet available. As of 2008, more than 500 clinical trials were investigating possible treatments for AD, but it is unknown if any of them will prove successful. Many measures have been suggested for the prevention of Alzheimer’s disease, but their value is unproven in slowing the course and reducing the severity of the disease.

Mental stimulation, exercise, and a balanced diet are often recommended, as both a possible prevention and a sensible way of managing the disease. Because AD cannot be cured and is degenerative, management of patients is essential. The role of the main caregiver is often taken by the spouse or a close relative. Alzheimer’s disease is known for placing a great burden on caregivers; the pressures can be wide-ranging, involving social, psychological, physical, and economic elements of the caregiver’s life. In developed countries, AD is one of the most economically costly diseases to society. The disease course is divided into four stages, with a progressive pattern of cognitive and functional impairment. Predementia The first symptoms are often mistaken as related to ageing or stress. Detailed neuropsychological testing can reveal mild cognitive difficulties up to eight years before a person fulfills the clinical criteria for diagnosis of AD. These early symptoms can affect the most complex daily living activities. The most noticeable deficit is memory loss, which shows up as difficulty in remembering recently learned facts and inability to acquire new information.

Subtle problems with the executive functions of attentiveness, planning, flexibility, and abstract thinking, or impairments in semantic memory (memory of meanings, and concept relationships), can also be symptomatic of the early stages of AD. Apathy can be observed at this stage, and remains the most persistent neuropsychiatric symptom throughout the course of the disease. The preclinical stage of the disease has also been termed mild cognitive impairment, but there is still debate on whether this term corresponds to a different diagnostic entity by itself or just a first step of the disease. Early dementia In people with AD the increasing impairment of learning and memory eventually leads to a definitive diagnosis. In a small proportion of them, difficulties with language, executive functions, perception (agnosia), or execution of movements (apraxia) are more prominent than memory problems. AD does not affect all memory capacities equally. Older memories of the person’s life (episodic memory), facts learned (semantic memory), and implicit memory (the memory of the body on how to do things, such as using a fork to eat) are affected to a lesser degree than new facts or memories.

Language problems are mainly characterised by a shrinking vocabulary and decreased word fluency, which lead to a general impoverishment of oral and written language. In this stage, the person with Alzheimer’s is usually capable of adequately communicating basic ideas. While performing fine motor tasks such as writing, drawing or dressing, certain movement coordination and planning difficulties (apraxia) may be present, making sufferers appear clumsy. As the disease progresses, people with AD can often continue to perform many tasks independently, but may need assistance or supervision with the most cognitively demanding activities. Moderate dementia Progressive deterioration eventually hinders independence. Speech difficulties become evident due to an inability to recall vocabulary, which leads to frequent incorrect word substitutions (paraphasias). Reading and writing skills are also progressively lost. Complex motor sequences become less coordinated as time passes, reducing the ability to perform most normal daily living activities. During this phase, memory problems worsen, and the person may fail to recognise close relatives. Long-term memory, which was previously intact, becomes impaired, and behavioural changes become more prevalent. Common neuropsychiatric manifestations are wandering, sundowning, irritability and labile affect, leading to crying, outbursts of unpremeditated aggression, or resistance to caregiving.

Approximately 30% of patients also develop illusionary misidentifications and other delusional symptoms. Urinary incontinence can develop. These symptoms create stress for relatives and caretakers, which can be reduced by moving the person from home care to other long-term care facilities. Advanced dementia During this last stage of AD, the patient is completely dependent upon caregivers. Language is reduced to simple phrases or even single words, eventually leading to complete loss of speech. Despite the loss of verbal language abilities, patients can often understand and return emotional signals. Although aggressiveness can still be present, extreme apathy and exhaustion are much more common results. Patients will ultimately not be able to perform even the most simple tasks without assistance. Muscle mass and mobility deteriorate to the point where they are bedridden, [47] and they lose the ability to feed themselves. Finally comes death, usually caused directly by some external factor such as pressure ulcers or pneumonia, not by the disease itself.

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Nutriceed Medical Systems, Inc. was founded by seven MD's, each in a different specialty. An estimated 26.6 million people worldwide had Alzheimer's in 2006; this number may quadruple by 2050. Although the course of Alzheimer's disease is unique for every individual, there are many common symptoms. The cause and progression of Alzheimer's disease are not well understood. Research indicates that the disease is associated with plaques and tangles in the brain. Currently used treatments offer a small symptomatic benefit; no treatments to delay or halt the progression of the disease are as yet available. Your Answer to Staying Young and Healthy! Alzheimer's Disease About Watch and Favorite Watch Watching this resources will notify you when proposed changes or new versions are created so you can keep track of improvements that have been made. Favorite Favoriting this resource allows you to save it in the “My Resources” tab of your account. There, you can easily access this resource later when you’re ready to customize it or assign it to your students. Alzheimer's Disease Alzheimer's disease is an age-linked neurodegenerative disorder characterized by marked dementia.

Learning Objective Describe Alzheimer's disease and its effect on the brain Key Points Alzheimer's disease (AD) is the most common form of dementia and was first described by German psychiatrist Alois Alzheimer in 1906. There is no cure for AD, which worsens as it progresses and eventually leads to death. Current treatments only help with the symptoms of the disease. A small number of cases of AD are inherited and usually have an onset before age 65. This form of the disease is known as early-onset familial AD. AD is associated with deposits of amyloid-beta peptide , called plaques , and aggregates of the microtubule-associated protein tau, called tangles, in the brain , which contribute to neuron death. Term A peptide of 36–43 amino acids that is processed from the Amyloid precursor protein, best known as a component of amyloid plaques in association with Alzheimer's disease. Example Examples of common symptoms of AD include difficulty remembering recent events and, as the disease advances, confusion, irritability, aggression, mood swings, trouble with language, and long-term memory loss. Register for FREE to remove ads and unlock more features!

Learn more Full Text Alzheimer's disease (AD), also known in medical literature as Alzheimer disease, is the most common form of dementia. There is no cure for the disease, which worsens as it progresses, and eventually leads to death. It was first described by German psychiatrist and neuropathologist Alois Alzheimer in 1906 and was named after him. Most often, AD is diagnosed in people over 65 years of age, although the less-prevalent early-onset Alzheimer's can occur much earlier. In 2006, there were 26.6 million sufferers worldwide. Alzheimer's is predicted to affect 1 in 85 people globally by 2050. Symptoms and Prognosis Although Alzheimer's disease develops differently for every individual, there are many common symptoms. Early symptoms are often mistakenly thought to be "age-related" concerns or manifestations of stress . In the early stages, the most common symptom is difficulty in remembering recent events. When AD is suspected, the diagnosis is usually confirmed with tests that evaluate behavior and thinking abilities, often followed by a brain scan if available.

As the disease advances, symptoms can include confusion, irritability, aggression, mood swings, trouble with language, and long-term memory loss. As the sufferer declines they often withdraw from family and society. Gradually, bodily functions are lost, ultimately leading to death. Since the disease is different for each individual, predicting how it will affect the person is difficult. AD develops for an unknown and variable amount of time before becoming fully apparent, and it can progress undiagnosed for years. On average, the life expectancy following diagnosis is approximately seven years. Fewer than three percent of individuals live more than fourteen years after diagnosis. Causes The cause for most Alzheimer's cases is still essentially unknown (except for 1% to 5% of cases where genetic differences have been identified). Several competing hypotheses exist trying to explain the cause of the disease. The oldest, on which most currently available drug therapies are based, is the cholinergic hypothesis, which proposes that AD is caused by reduced synthesis of the neurotransmitter acetylcholine . The cholinergic hypothesis has not maintained widespread support, largely because medications intended to treat acetylcholine deficiency have not been very effective.

Other cholinergic effects have also been proposed, for example, initiation of large-scale aggregation of amyloid, leading to generalized neuroinflammation. In 1991, the amyloid hypothesis postulated that amyloid beta (Aβ) deposits are the fundamental cause of the disease. Support for this postulate comes from the location of the gene for the amyloid beta precursor protein (APP) on chromosome 21, together with the fact that people with trisomy 21 (Down syndrome) who have an extra gene copy almost universally exhibit AD by 40 years of age. Also APOE4, the major genetic risk factor for AD, leads to excess amyloid buildup in the brain. Further evidence comes from the finding that transgenic mice that express a mutant form of the human APP gene develop fibrillar amyloid plaques and Alzheimer's-like brain pathology with spatial learning deficits.

Question: Which form of dementia is named after a German psychiatrist who first described it in 1906?
Answer: Alzheimer's Disease